F10 Fraction Of Terminalia Arjuna (TA) Bark Aqueous Extract Exerts A Positive Inotropic Effect On Adult Ventricular Myocytes

Planta Medica ◽  
2016 ◽  
Vol 82 (05) ◽  
Author(s):  
SJ Liu ◽  
G Zheng ◽  
PA Crooks
Keyword(s):  
Aqueous Extract ◽  
Positive Inotropic Effect ◽  
Ventricular Myocytes ◽  
Inotropic Effect ◽  
Terminalia Arjuna

Mechanical and electrophysiological effects of a hydroxyphenyl-substituted tetrahydroisoquinoline, SL-1, on isolated rat cardiac tissues

1995 ◽  
Vol 73 (11) ◽  
pp. 1651-1660 ◽  
Author(s):  
Gwo-Jyh Chang ◽  
Ming-Jai Su ◽  
Pei-Hong Lee ◽  
Shoei-Sheng Lee ◽  
Karin Chiung-Sheue Liu
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Positive Inotropic Effect ◽  
Ventricular Myocytes ◽  
Inotropic Effect ◽  
Dependent Manner ◽  
Cardiac Tissues ◽  
Inward Current ◽  
Adrenoceptor Antagonist ◽  
Isolated Rat

The mechanisms of the positive inotropic action of a new synthetic tetrahydroisoquinoline compound, SL-1, were investigated in isolated rat cardiac tissues and ventricular myocytes. SL-1 produced a rapidly developing, concentration-dependent positive inotropic response in both atrial and ventricular muscles and a negative chronotropic effect in spontaneously beating right atria. The positive inotropic effect was not prevented by pretreatment with reserpine (3 mg/kg) or the α-adrenoceptor antagonist prazosin (1 μM), but was suppressed by either the β-adrenoceptor antagonist atenolol (3 μM) or the K+ channel blocker 4-aminopyridine (4AP, 1 mM). In the whole-cell recording study, SL-1 increased the plateau level and prolonged the action potential duration in a concentration-dependent manner and decreased the maximum upstroke velocity [Formula: see text] and amplitude of the action potential in isolated rat ventricular myocytes stimulated at 1.0 Hz. On the other hand, SL-1 had little effect on the resting membrane potential, although it caused a slight decrease at higher concentrations. Voltage clamp experiments revealed that the increase of action potential plateau and prolongation of action potential duration were associated with an increase of Ca2+ inward current (ICa) via the activation of β-adrenoceptors and a prominent inhibition of 4AP-sensitive transient outward K+ current (Ito) with an IC50 of 3.9 μM. Currents through the inward rectifier K+ channel (IKl) were also reduced. The inhibition of Ito is characterized by a reduction in peak amplitude and a marked acceleration of current decay but without changes on the voltage dependence of steady-state inactivation. In addition to the inhibition of K+ currents, SL-1 also inhibited the Na+ inward current (INa) with an IC50 of 5.4 μM, which was correlated with the decrease of [Formula: see text]. We conclude that the positive inotropic effect of SL-1 may be due to an increase in Ca2+ current mediated via partial activation of β-adrenoceptors and an inhibition of K+ outward currents and the subsequent prolongation of action potentials.Key words: SL-1, tetrahydroisoquinoline, inotropic and chronotropic action, action potential, Na+, Ca2+, and K+ currents.

Antagonistic Actions of Halothane and Sevoflurane on Spontaneous Ca2+Release in Rat Ventricular Myocytes

2006 ◽  
Vol 105 (1) ◽  
pp. 58-64 ◽  
Author(s):  
Mark D. Graham ◽  
Philip M. Hopkins ◽  
Simon M. Harrison
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Positive Inotropic Effect ◽  
Ventricular Myocytes ◽  
Inotropic Effect ◽  
Release Process ◽  
Rat Ventricular Myocytes ◽  
Fura 2 ◽  
Threefold Increase ◽  
Subcellular Target ◽  
Isolated Rat

Background Halothane has been reported to sensitize Ca(2+) release from the sarcoplasmic reticulum (SR), which is thought to contribute to its initial positive inotropic effect. However, little is known about whether isoflurane or sevoflurane affect the SR Ca(2+) release process, which may contribute to the inotropic profile of these anesthetics. Methods Mild Ca(2+) overload was induced in isolated rat ventricular myocytes by increase of extracellular Ca(2+) to 2 mM. The resultant Ca(2+) transients due to spontaneous Ca(2+) release from the SR were detected optically (fura-2). Cells were exposed to 0.6 mM anesthetic for a period of 4 min, and the frequency and amplitude of spontaneous Ca(2+) transients were measured. Results Halothane caused a temporary threefold increase in frequency and decreased the amplitude (to 54% of control) of spontaneous Ca(2+) transients. Removal of halothane inhibited spontaneous Ca release before it returned to control. In contrast, sevoflurane initially inhibited frequency of Ca(2+) release (to 10% of control), whereas its removal induced a burst of spontaneous Ca(2+) release. Isoflurane had no significant effect on either frequency or amplitude of spontaneous Ca(2+) release on application or removal. Sevoflurane was able to ameliorate the effects of halothane on the frequency and amplitude of spontaneous Ca(2+) release both on application and wash-off. Conclusions Application of halothane and removal of sevoflurane sensitize the SR Ca(2+) release process (and vice versa on removal). Sevoflurane reversed the effects of halothane, suggesting they may act at the same subcellular target on the SR.

The positive inotropic effect of the aqueous extract of Convallaria keiskei in beating rabbit atria

Life Sciences ◽  
2006 ◽  
Vol 79 (12) ◽  
pp. 1178-1185 ◽  
Author(s):  
Deok Ho Choi ◽  
Dae Gill Kang ◽  
Xun Cui ◽  
Kyung Woo Cho ◽  
Eun Jin Sohn ◽  
...  
Keyword(s):  
Aqueous Extract ◽  
Positive Inotropic Effect ◽  
Inotropic Effect ◽  
Rabbit Atria

scholarly journals Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes

2015 ◽  
Vol 24 (4) ◽  
pp. 236-240 ◽  
Author(s):  
Alejandra M. Yeves ◽  
Claudia I. Caldiz ◽  
Ernesto A. Aiello ◽  
María C. Villa-Abrille ◽  
Irene L. Ennis
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Positive Inotropic Effect ◽  
Ventricular Myocytes ◽  
Reactive Oxygen ◽  
Inotropic Effect ◽  
High Dose ◽  
Oxygen Species

A novel phospholipase C- and cAMP-independent positive inotropic mechanism via a P2 purinoceptor

1997 ◽  
Vol 273 (5) ◽  
pp. H2380-H2387 ◽  
Author(s):  
Ernest Podrasky ◽  
David Xu ◽  
Bruce T. Liang
Keyword(s):  
Phospholipase C ◽  
Positive Inotropic Effect ◽  
Ventricular Myocytes ◽  
Inositol Phosphates ◽  
Inotropic Effect ◽  
Maximal Increase ◽  
Cyclic Monophosphate ◽  
Myocyte Contractility ◽  
Novel Model ◽  
Potency Order

Although ATP, acting through a P2 purinoceptor, can stimulate a pronounced positive inotropic effect in cardiac ventricular myocytes, the receptor-effector mechanism that underlies this stimulatory cardiac action is not well understood. The objectives of the present study were to develop the cultured chick embryo ventricular myocytes as a novel model for the cardiac P2 purinoceptor and to determine the mechanism underlying its positive inotropic effect. ATP caused an 89 ± 8.9% ( n = 14 cells) increase in the myocyte contractility, with an efficacy and potency order of ATP > ADP > AMP ≫ adenosine. 2-Methylthio-ATP (2-MeS-ATP) but not α,β-methylene-ATP was able to stimulate myocyte contractility, with a maximal increase of 54 ± 2.6% ( n = 11 cells). Although UTP potently stimulates phosphoinositide hydrolysis, it had an only modest positive inotropic effect (27 ± 7% maximal increase; n = 8 cells). In contrast to previous suggestions, the 2-MeS-ATP-stimulated positive inotropic response does not require the action of phospholipase C (PLC), such as that of the inositol phosphates; the UTP effect on contractility appears to be mediated via the 2-MeS-ATP-sensitive P2 receptor. The PLC inhibitor U-73122 had no effect on the 2-MeS-ATP-stimulated increase in contractility, providing further evidence against a role for PLC in the inotropic effect of 2-MeS-ATP. An adenosine 3′,5′-cyclic monophosphate-independent Ca2+ entry-stimulating mechanism appears to underlie a direct coupling of the receptor to stimulation of the myocyte contractility. This new PLC- and adenosine 3′,5′-cyclic monophosphate-independent positive inotropic mechanism represents a target for developing novel positive inotropic therapeutics.

scholarly journals An aqueous extract of Zanthoxylum schinifolium has a positive inotropic effect in beating rabbit atria

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Hao Zhen Cui ◽  
Dae Gill Kang ◽  
Seung Ju Kim ◽  
Deok Ho Choi ◽  
Kyung Woo Cho ◽  
...  
Keyword(s):  
Aqueous Extract ◽  
Positive Inotropic Effect ◽  
Inotropic Effect ◽  
Zanthoxylum Schinifolium ◽  
Rabbit Atria

Effects of phenylephrine on calcium current and contractility of feline ventricular myocytes

1988 ◽  
Vol 255 (5) ◽  
pp. H1173-H1180 ◽  
Author(s):  
H. A. Hartmann ◽  
N. J. Mazzocca ◽  
R. B. Kleiman ◽  
S. R. Houser
Keyword(s):  
Calcium Current ◽  
Positive Inotropic Effect ◽  
Ventricular Myocytes ◽  
Inotropic Effect ◽  
Receptor Blockade ◽  
Receptor Stimulation ◽  
Contractile State ◽  
Kinase C ◽  
Beta Receptor Blockade ◽  
Stimulation Of

Previous studies on numerous cardiac preparations have shown that stimulation of alpha 1-receptors produces a positive inotropic effect. The cellular basis for this effect is not well understood. Isolated feline ventricular myocytes were used in the present study to examine the idea that the increase in contractility induced by stimulation of alpha 1-receptors is produced by an increase in inward Ca2+ current and that this event is caused by the stimulation of protein kinase C (PKC). These experiments showed that phenylephrine (10(-4) M) increased Ca2+ current from 0.56 +/- 0.02 (control) to 1.12 +/- 0.25 nA and increased contractile magnitude by 201 +/- 28%. The effect on Ca2+ current was completely blocked by propranolol (10(-7)M), whereas after beta-receptor blockade, contractile state was still 130 +/- 8% of control levels. alpha 1-Receptor blockade by prazosin eliminated this residual inotropic component of phenylephrine. Lower concentrations of phenylephrine (10(-7)M) were without effect on Ca2+ current and contractility as was stimulation of PCK with 150 nM of a phorbol ester. These results suggest that the positive inotropic effect of alpha 1-receptor stimulation in adult feline ventricular myocytes is not produced by increasing inward Ca2+ current and that this response is also not associated with stimulation of PKC.

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